Enterocolitis inducida por proteínas de pescado

La enterocolitis inducida por proteínas de la dieta (EIPD) es una alergia gastrointestinal no mediada por IgE que cursa con manifestaciones exclusivamente digestivas y que aparece, fundamentalmente, en la infancia. Las manifestaciones clínicas de la EIPD son vómitos tardíos recurrentes, diarrea, letargo, palidez e hipotensión que pueden progresar a un estado de deshidratación y shock hipovolémico. Los síntomas se repiten cada vez que el niño consume el alimento causal y desaparecen una vez que éste es retirado de la dieta. Los alimentos más frecuentemente implicados en esta enfermedad son la leche de vaca y la soja. Entre los alimentos sólidos destaca el arroz, sin embargo, existen diferencias en función del área geográfica. En la zona mediterránea, el pescado es el alimento que con más frecuencia produce EIPD. El pronóstico de la EIPD depende del alimento causal y en el caso de la enterocolitis inducida por proteínas de pescado, éste no parece tan favorable y no siempre se supera la enfermedad. El único tratamiento disponible actualmente es la evitación del alimento responsable de los síntomas. En nuestro medio, eso implica que los niños deben realizar una dieta completamente exenta de pescado hasta la resolución de la enfermedad. No existe ningún marcador diagnóstico ni pronóstico de la evolución de la enfermedad, por lo tanto, todos los niños deben pasar por una prueba de exposición oral controlada (PEOC) con el alimento causal al menos en una ocasión. Esta prueba no está exenta de riesgos pudiendo desencadenar síntomas moderados y graves tras la misma. El objetivo del presente estudio fue establecer la necesidad o no de la realización de una dieta completamente exenta de pescado en el caso de los niños diagnosticados de EIPD, así como establecer una metodología más segura y eficaz para la realización de la PEOC. Realizamos un estudio ambispectivo y observacional, en el que se incluyeron todos los niños diagnosticados de enterocolitis por pescado en un periodo de 20 años. Se recogieron las características demográficas y clínicas, los pescados más frecuentemente implicados en el inicio, y la edad de tolerancia completa (tolerancia a todos los pescados) o parcial (tolerancia a algún pescado diferente filogenéticamente del implicado). Se recogieron los pescados que fueron mejor tolerados por los niños que no superaron por completo la enfermedad. Se realizó una PEOC en aquellos casos en los que estaba indicada con finalidad diagnóstica y, durante el seguimiento, para comprobar si se había superado o no la enfermedad o para procurar una alternativa dietética. La PEOC se realizó siguiendo dos metodologías diferentes. Comparamos los dos métodos con el fin de evaluar el perfil de seguridad y establecer si había diferencia en la gravedad de los síntomas presentados en función de cómo se realizó la prueba. El Método 1 consistió en dar dosis crecientes del alimento cada 30 minutos, consumiéndose la ración completa en el mismo día, y el Método 2 que consistió en dar una dosis única al día en 2 o 3 días no consecutivos. Se incluyeron 80 niños en el estudio con una mediana de edad al comienzo de los síntomas de 10 meses. Los pescados más frecuentemente implicados en el comienzo de la enfermedad fueron merluza, gallo y lenguado y los mejor tolerados por aquellos niños que no superaron por completo la enfermedad o que alcanzaron la tolerancia parcial antes que la completa, fueron el atún en conserva y el pez espada, fundamentalmente. El 76% de los niños alcanzaron algún tipo de tolerancia. La edad de tolerancia completa en nuestra población fue de cuatro años mientras que la edad de tolerancia parcial fue de tres años. Cuando analizamos la metodología de la PEOC objetivamos que sí hay diferencias en el perfil de seguridad y en cuanto a la gravedad de los síntomas en función de si la ración completa se administró en un solo día o fraccionada en varios días, que es el método propuesto en nuestro estudio. Con este trabajo podemos concluir que, no es necesario realizar una dieta completamente restrictiva en el caso de los niños con enterocolitis inducida por proteínas de pescado, ya que hay algunos pescados que pueden ser tolerados, y que con la metodología para la PEOC propuesta en el presente estudio se mejora la seguridad de la prueba

Children with acute food protein-induced enterocolitis syndrome from Spain and Italy usually tolerate all other food groups.

Acute food protein-induced enterocolitis syndrome ('FPIES') is a potentially severe type of non IgE-mediated food allergy affecting mainly infants usually when foods are introduced [1]. Acute FPIES triggered by multiple unrelated foods ('multiple food FPIES') has been reported in up to two thirds of patients, particularly in the USA [2,3]. FPIES reactions are often traumatic experiences for parents and weaning leads to significant anxiety, as there is no test to identify safe new foods. This has led to complex weaning recommendations in children with FPIES in an attempt to support parents [4]. However, evidence suggests that multiple food FPIES is rare in other regions, such as Southern Europe [5,6], which questions the applicability of such weaning advice in this population. Studies including a detailed dietary history in children with FPIES are lacking

SARS-CoV-2 viral load in nasopharyngeal swabs is not an independent predictor of unfavorable outcome

The aim was to assess the ability of nasopharyngeal SARS-CoV-2 viral load at frst patient’s hospital evaluation to predict unfavorable outcomes. We conducted a prospective cohort study including 321 adult patients with confrmed COVID-19 through RT-PCR in nasopharyngeal swabs. Quantitative Synthetic SARS-CoV-2 RNA cycle threshold values were used to calculate the viral load in log10 copies/mL. Disease severity at the end of follow up was categorized into mild, moderate, and severe. Primary endpoint was a composite of intensive care unit (ICU) admission and/or death (n= 85, 26.4%). Univariable and multivariable logistic regression analyses were performed. Nasopharyngeal SARS-CoV-2 viral load over the second quartile (≥7.35 log10 copies/mL, p = 0.003) and second tertile (≥ 8.27 log10 copies/mL, p = 0.01) were associated to unfavorable outcome in the unadjusted logistic regression analysis. However, in the fnal multivariable analysis, viral load was not independently associated with an unfavorable outcome. Five predictors were independently associated with increased odds of ICU admission and/or death: age≥ 70 years, SpO2, neutrophils > 7.5 × ­103 /µL, lactate dehydrogenase≥ 300 U/L, and C-reactive protein≥ 100 mg/L. In summary, nasopharyngeal SARS-CoV-2 viral load on admission is generally high in patients with COVID-19, regardless of illness severity, but it cannot be used as an independent predictor of unfavorable clinical outcome

SARS-CoV-2 viral load in nasopharyngeal swabs is not an independent predictor of unfavorable outcome

The aim was to assess the ability of nasopharyngeal SARS-CoV-2 viral load at first patient’s hospital evaluation to predict unfavorable outcomes. We conducted a prospective cohort study including 321 adult patients with confirmed COVID-19 through RT-PCR in nasopharyngeal swabs. Quantitative Synthetic SARS-CoV-2 RNA cycle threshold values were used to calculate the viral load in log10 copies/mL. Disease severity at the end of follow up was categorized into mild, moderate, and severe. Primary endpoint was a composite of intensive care unit (ICU) admission and/or death (n = 85, 26.4%). Univariable and multivariable logistic regression analyses were performed. Nasopharyngeal SARS-CoV-2 viral load over the second quartile (≥ 7.35 log10 copies/mL, p = 0.003) and second tertile (≥ 8.27 log10 copies/mL, p = 0.01) were associated to unfavorable outcome in the unadjusted logistic regression analysis. However, in the final multivariable analysis, viral load was not independently associated with an unfavorable outcome. Five predictors were independently associated with increased odds of ICU admission and/or death: age ≥ 70 years, SpO2, neutrophils > 7.5 × 103/µL, lactate dehydrogenase ≥ 300 U/L, and C-reactive protein ≥ 100 mg/L. In summary, nasopharyngeal SARS-CoV-2 viral load on admission is generally high in patients with COVID-19, regardless of illness severity, but it cannot be used as an independent predictor of unfavorable clinical outcome

Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection

Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components. Dendritic cells (DCs) play a key role in the defense against viral infections, for instance plasmacytoid DCs (pDCs), have the capacity to produce vast amounts of interferon-alpha (IFN-α). In COVID-19 there is a deficit in DC numbers and IFN-α production, which has been associated with disease severity. In this work, we described that in addition to the DC deficiency, several DC activation and homing markers were altered in acute COVID-19 patients, which were associated with multiple inflammatory markers. Remarkably, previously hospitalized and nonhospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection. Moreover, the expression of DC markers such as CD86 and CD4 were only restored in previously nonhospitalized patients, while no restoration of integrin β7 and indoleamine 2,3-dyoxigenase (IDO) levels were observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19

Treatment with tocilizumab or corticosteroids for COVID-19 patients with hyperinflammatory state: a multicentre cohort study (SAM-COVID-19)

Objectives: The objective of this study was to estimate the association between tocilizumab or corticosteroids and the risk of intubation or death in patients with coronavirus disease 19 (COVID-19) with a hyperinflammatory state according to clinical and laboratory parameters. Methods: A cohort study was performed in 60 Spanish hospitals including 778 patients with COVID-19 and clinical and laboratory data indicative of a hyperinflammatory state. Treatment was mainly with tocilizumab, an intermediate-high dose of corticosteroids (IHDC), a pulse dose of corticosteroids (PDC), combination therapy, or no treatment. Primary outcome was intubation or death; follow-up was 21 days. Propensity score-adjusted estimations using Cox regression (logistic regression if needed) were calculated. Propensity scores were used as confounders, matching variables and for the inverse probability of treatment weights (IPTWs). Results: In all, 88, 117, 78 and 151 patients treated with tocilizumab, IHDC, PDC, and combination therapy, respectively, were compared with 344 untreated patients. The primary endpoint occurred in 10 (11.4%), 27 (23.1%), 12 (15.4%), 40 (25.6%) and 69 (21.1%), respectively. The IPTW-based hazard ratios (odds ratio for combination therapy) for the primary endpoint were 0.32 (95%CI 0.22-0.47; p < 0.001) for tocilizumab, 0.82 (0.71-1.30; p 0.82) for IHDC, 0.61 (0.43-0.86; p 0.006) for PDC, and 1.17 (0.86-1.58; p 0.30) for combination therapy. Other applications of the propensity score provided similar results, but were not significant for PDC. Tocilizumab was also associated with lower hazard of death alone in IPTW analysis (0.07; 0.02-0.17; p < 0.001). Conclusions: Tocilizumab might be useful in COVID-19 patients with a hyperinflammatory state and should be prioritized for randomized trials in this situatio

{IgE}-mediated fish allergy in pediatric age: Does canned tuna have a chance for tolerance?

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Non-IgE-Mediated Gastrointestinal Food Protein-Induced Allergic Disorders. Clinical Perspectives and Analytical Approaches

Non-IgE-mediated gastrointestinal food allergy (non-IgE-GI-FA) is the name given to a series of pathologies whose main entities are food protein-induced allergic proctocolitis (FPIAP), food protein-induced enteropathy (FPE), and food protein-induced enterocolitis syndrome (FPIES). These are more uncommon than IgE-mediated food allergies, their mechanisms remain largely unknown, and their diagnosis is mainly done by clinical history, due to the lack of specific biomarkers. In this review, we present the latest advances found in the literature about clinical aspects, the current diagnosis, and treatment options of non-IgE-GI-FAs. We discuss the use of animal models, the analysis of gut microbiota, omics techniques, and fecal proteins with a focus on understanding the pathophysiological mechanisms of these pathologies and obtaining possible diagnostic and/or prognostic biomarkers. Finally, we discuss the unmet needs that researchers should tackle to advance in the knowledge of these barely explored pathologies